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目的探讨高压氧(HBO)对新生大鼠缺氧缺血性脑损伤(HIBD)模型脑组织神经细胞凋亡和超氧化物歧化酶(SOD)、脂质过氧化物(MDA)的影响。方法新生7d龄健康SD大鼠随机分为4组:空白对照组(n=68),假手术组(分离左颈总动脉后不结扎直接缝合皮肤,n=66),HIBD组(模型制作采用经典的Rice法,n=60),HBO组(HIBD后行HBO治疗,1h/次/d,最长治疗7d,n=66)。TUNEL试剂盒检测脑组织凋亡的神经细胞,黄嘌呤氧化酶法测定SOD活力(nU/ml)和化学比色法测定MDA含量(μmol/L)。结果(1)缺氧缺血后不同时间HIBD组皮质和海马神经细胞凋亡明显增多,24h达高峰后逐渐下降;HBO组凋亡细胞数较HIBD组明显减少,但仍较空白对照组和假手术组高,差异有统计学意义(P<0.05);(2)缺氧缺血后HIBD组SOD含量下降,HBO治疗后SOD的含量较HIBD组升高,且随着治疗时间的延长SOD的水平逐渐升高,24h达高峰,然后逐渐下降,各组比较差异有统计学意义(P<0.05);(3)缺氧缺血后HIBD组MDA含量明显升高,18至24h达高峰,随着时间的推移逐渐下降;HBO治疗后MDA含量较HIBD组明显降低,差异有统计学意义(P<0.05)。结论HBO治疗可减轻HIBD后神经细胞凋亡,机制可能与HBO诱导脑组织SOD的表达,增强组织的抗氧化应激损伤有关。
Objective To investigate the effects of hyperbaric oxygen (HBO) on neuronal apoptosis and superoxidase dismutase (SOD) and lipid peroxidase (MDA) in the brain of hypoxic-ischemic brain damage (HIBD) model of neonatal rats. Methods Newborn 7-day-old SD rats were randomly divided into 4 groups: blank control group (n = 68), sham operation group (without left common carotid artery ligated directly sutured skin, n = 66), HIBD group The classic Rice method, n = 60), HBO group (HBO HBO after treatment, 1h / time / d, the longest treatment of 7d, n = 66). TUNEL kit was used to detect neuronal apoptosis in brain tissue. SOD activity (nU / ml) was measured by xanthine oxidase method and MDA content (μmol / L) was measured by chemical colorimetry. Results (1) The apoptosis of cortex and hippocampus neurons in HIBD group increased significantly at different time points after hypoxia-ischemia, and gradually decreased after reaching the peak at 24 h. The number of apoptotic cells in HIBD group decreased significantly compared with HIBD group, (2) The content of SOD in HIBD group decreased after hypoxia-ischemia, the content of SOD in HIBD group increased after HBO treatment, and with the prolongation of treatment time, the content of SOD (P <0.05). (3) The content of MDA in HIBD group increased significantly after hypoxia-ischemia and peaked at 18 to 24h, with the increase of With the passage of time gradually decreased; HBO treatment MDA content was significantly lower than the HIBD group, the difference was statistically significant (P <0.05). Conclusions HBO treatment can reduce the apoptosis of neural cells after HIBD. The mechanism may be related to HBO inducing the expression of SOD in brain tissue and enhancing the anti-oxidative stress injury of the tissue.